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T-bet is required for optimal proinflammatory CD4+ T-cell trafficking.

ABSTRACT: Inflammatory responses are controlled by T helper 1 (Th1) lymphocytes. An important function of this polarity is the ability of T cells to traffick appropriately in vivo. This differential trafficking is dependent upon the binding of P-selectin glycoprotein ligand-1 to P- and E-selectin on inflamed endothelium as well as the expression of specific chemokine receptors. Here we show that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abrogated and that T-bet regulates the binding of CD4(+) T cells to P-selectin. T-bet is also required for the expression of the chemokine receptor CXCR3. Thus, T-bet controls Th1-cell migration to inflammatory sites, which has fundamental consequences for the control of immunologic disease.

SUBMITTER: Lord GM

PROVIDER: S-EPMC1895048 | biostudies-literature | 2005 Nov

REPOSITORIES: biostudies-literature

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T-bet is required for optimal proinflammatory CD4+ T-cell trafficking.

Lord Graham M GM Rao Ravi M RM Choe Hyeryun H Sullivan Brandon M BM Lichtman Andrew H AH Luscinskas F William FW Glimcher Laurie H LH

Blood 20050712 10

Inflammatory responses are controlled by T helper 1 (Th1) lymphocytes. An important function of this polarity is the ability of T cells to traffick appropriately in vivo. This differential trafficking is dependent upon the binding of P-selectin glycoprotein ligand-1 to P- and E-selectin on inflamed endothelium as well as the expression of specific chemokine receptors. Here we show that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abro ...[more]

PMID: 16014561

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